TaADF3, an Actin-Depolymerizing Factor, Negatively Modulates Wheat Resistance Against Puccinia striiformis.
TaADF3, an Actin-Depolymerizing Factor, Negatively Modulates Wheat Resistance Against Puccinia striiformis.
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DOI：
10.3389/fpls.2015.01214
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发表时间：
2015
影响因子：
5.6
通讯作者：
Kang Z
中科院分区：
文献类型：
--
作者：
Tang C;Deng L;Chang D;Chen S;Wang X;Kang Z
肌动蛋白细胞骨架与植物抵御病原真菌、卵菌和细菌的防御有关。肌动蛋白解聚因子(ADF)是一种刺激反应型肌动蛋白细胞骨架调节剂。然而，将ADF与植物抵御病原体联系起来的证据有限。在本研究中，我们从小麦中分离到了一个逆境响应ADF基因(TaADF3)，并对其进行了功能鉴定，该基因在所有被检测的小麦组织中都能检测到。TaADF3是一个三拷贝基因，位于染色体5AL、5BL和5DL上。洋葱表皮细胞的粒子轰击实验表明，TaADF3在细胞质和核中均有定位。TaADF3的表达受脱落酸(ABA)、各种非生物胁迫(干旱和低温)和条锈菌毒力的诱导。小黑麦(Tritici，PST)，但在无毒的PST诱导下表达下调。病毒诱导的TaADF3拷贝沉默增强了小麦对无毒PST的抗性，降低了ROS积累和过敏性反应(HR)。经强毒PST处理后，TaADF3基因敲除植株表现出较低的感受性，同时伴随着ROS的产生和HR的增加。有趣的是，TaADF3的沉默导致无毒和致病PST的病原菌穿透和吸器形成受阻。此外，在TaADF3基因敲除的表皮细胞中，肌动蛋白细丝的排列和分布发生了变化，这可能有助于减弱真菌的穿透。因此，我们的发现表明，TaADF3以一种ROS依赖的方式正向调节小麦对非生物胁迫的耐受性，而以一种ROS依赖的方式负向调节小麦对PST的抗性，这可能是依赖肌动蛋白结构动态阻止真菌穿透的机制。
The actin cytoskeleton has been implicated in plant defense against pathogenic fungi, oomycetes, and bacteria. Actin depolymerizing factors (ADFs) are stimulus responsive actin cytoskeleton modulators. However, there is limited evidence linking ADFs with plant defense against pathogens. In this study, we have isolated and functionally characterized a stress-responsive ADF gene (TaADF3) from wheat, which was detectable in all examined wheat tissues. TaADF3 is a three-copy gene located on chromosomes 5AL, 5BL, and 5DL. A particle bombardment assay in onion epidermal cells revealed the cytoplasmic and nuclear localization of TaADF3. The expression of TaADF3 was inducible by abscisic acid (ABA), as well as various abiotic stresses (drought and cold) and virulent Puccinia striiformis f. sp. tritici (Pst) but was down regulated in response to avirulent Pst. Virus-induced silencing of TaADF3 copies enhanced wheat resistance to avirulent Pst, with decreased reactive oxygen species (ROS) accumulation and hypersensitive response (HR). Upon treatment with virulent Pst, TaADF3-knockdown plants exhibited reduced susceptibility, which was accompanied by increased ROS production and HR. Interestingly, the silencing of TaADF3 resulted in hindered pathogen penetration and haustoria formation for both avirulent and virulent Pst. Moreover, the array and distribution of actin filaments was transformed in TaADF3-knockdown epidermal cells, which possibly facilitated attenuating the fungus penetration. Thus, our findings suggest that TaADF3 positively regulates wheat tolerance to abiotic stresses and negatively regulates wheat resistance to Pst in an ROS-dependent manner, possibly underlying the mechanism of impeding fungal penetration dependent on the actin architecture dynamics.